40 replies to this topic

[1jol1uvcaaq]

 Like carbon monoxide spilling into a room of pure air, veganism theories have contaminated our minds with fantasies of a false health. Eating a high protein diet throughout history, humans have intriguingly gone astray from their god-given diet to a diet unknown to our bodies in the quest for a momentary satisfaction. When nutrient density is replaced with high-sugar, high-calorie foods, the immune system is be compromised, fighting off the naturally occuring allergens in grains, fruits, and starches. Beginning at the colon by promoting fermentation, constipation, and finally mucoid plaque, starch produces disease that slowly spreads to the brain, heart, liver, skin, joints,and hair after the body can no longer handle the stress.

 Our capitalistic desires have enclosed us in a prison that incapacitates our freewill to exercise the optimal human diet. Once our irresponsible cravings have been cured and our minds have been exposed to the truth, the prison is the truer difficulty in transitioning into a balanced diet. Nevertheless, if you are not reaching for improvement, your life is going nowhere.

 

 

My final word to you is to understand that carbohydrate cravings are detoxification, the same process a drug addict goes after quitting their poison. The road is not simple, but that's the beauty of life.

Edited by 1jol1uvcaaq, 12 January 2016 - 05:00 AM.

[1jol1uvcaaq]

Edit: The ketogenic diet is one of the greatest things that ever happened in health. Besides stemming from the already healthy and powerful paleolithic diet, the ketogenic diet actually experiments with the human body and health. It goes against the mainstream idea of health and attempts to reach beyond what we think is capable. I am one of those people who are not settling with the best we have right now, but are climbing to the heavens.

 

I understand not everybody is interested in true health, but the more ketogenic foods you eat, the healthier you are. You need to choose your path.

[niner]

I'm just waiting for MisterE to weigh in...

[Darryl]

No long-lived human population has consumed a ketogenic diet. The Inuit are neither long-lived, nor particularly immune to cardiometabolic disease.

 

While it possible that humans may have better adaptations to high fat or protein diets than our fellow extant Euarchontoglires, who for the past 95 million years have almost universally eaten very low fat and moderate protein diets, in practice human populations that consume higher fat diets develop cardiometabolic disease, and those that consume higher protein diets appear to have greater cancer mortality, pretty much the pattern observed in animal experiments.

 

Solon-Biet SM et al. 2014. The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. Cell metabolism, 19(3), pp.418-430.

 

 

 

Its also true no long-lived human population has consumed a vegan diet, though some have consumed less than 5% of calories from animal sources.

 

Willcox DC et al. 2009. The Okinawan diet: health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load. Journal of the American College of Nutrition, 28(sup4), pp.500S-516S.

 

Ignoring the serious and relatively recently solved issue of B12 sufficiency, there appears little health effect of a vegan diet versus the very low animal product diets consumed in the long-lived Blue Zones (marginal issues with antigen incorporation, eg Neu5gc and related autoimmune disorders). 

 

There probably isn't going to be conclusive evidence for an ideal longevity-promoting diet in the decades those of us alive today have left to take advantage of it. We can only follow the research, and adopt diets that resemble those that reduce age-associated diseases in large human populations, especially where they are supported by evidence from long-term animal feeding trials. For me, that means a predominantly whole plant based diet, high in fiber, resistant starch, hormetic and inflammation modulating phytochemicals, and low in calorie density, long-chain saturated fats, methionine (ie animal protein), and refined carbohydrates/glycemic index/added sugars. Whether one further restricts this whole plant based diet to a (B12 supplemented!) vegan diet is more of an ethical decision than one based on health evidence.

 

I also see some role for ketogenic diets, though I see little net health benefit except in the cases of diagnosed metastatic cancer, intractable epilepsy, or morbid obesity.

 

 

[aza]

Darryl, apparently not even the Inuit were in ketosis. They ate around 15-20% carbs from a few plant foods and animal glycogen and ate a lot of protein as well.

Edited by aza, 13 January 2016 - 11:34 AM.

[platypus]

Ketogenic diet is an extreme diet, I would do it if I had cancer though.

[1jol1uvcaaq]

No long-lived human population has consumed a ketogenic diet. The Inuit are neither long-lived, nor particularly immune to cardiometabolic disease.

 

While it possible that humans may have better adaptations to high fat or protein diets than our fellow extant Euarchontoglires, who for the past 95 million years have almost universally eaten very low fat and moderate protein diets, in practice human populations that consume higher fat diets develop cardiometabolic disease, and those that consume higher protein diets appear to have greater cancer mortality, pretty much the pattern observed in animal experiments.

 

Solon-Biet SM et al. 2014. The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. Cell metabolism, 19(3), pp.418-430.

 

 

 

Its also true no long-lived human population has consumed a vegan diet, though some have consumed less than 5% of calories from animal sources.

 

Willcox DC et al. 2009. The Okinawan diet: health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load. Journal of the American College of Nutrition, 28(sup4), pp.500S-516S.

 

Ignoring the serious and relatively recently solved issue of B12 sufficiency, there appears little health effect of a vegan diet versus the very low animal product diets consumed in the long-lived Blue Zones (marginal issues with antigen incorporation, eg Neu5gc and related autoimmune disorders). 

 

There probably isn't going to be conclusive evidence for an ideal longevity-promoting diet in the decades those of us alive today have left to take advantage of it. We can only follow the research, and adopt diets that resemble those that reduce age-associated diseases in large human populations, especially where they are supported by evidence from long-term animal feeding trials. For me, that means a predominantly whole plant based diet, high in fiber, resistant starch, hormetic and inflammation modulating phytochemicals, and low in calorie density, long-chain saturated fats, methionine (ie animal protein), and refined carbohydrates/glycemic index/added sugars. Whether one further restricts this whole plant based diet to a (B12 supplemented!) vegan diet is more of an ethical decision than one based on health evidence.

 

I also see some role for ketogenic diets, though I see little net health benefit except in the cases of diagnosed metastatic cancer, intractable epilepsy, or morbid obesity.

You can not compare a ketogenic diet to the  processed S.A.D. diet.

After I spent 40 days in a fasting retreat, my body could no longer handle high-phytochemical foods because of the deep detoxification I went through. Phytochemicals are healthy, but should be used as medicine, the way God intended for us to use them.

http://www.healthy-e...ns-in-food.html This list is missing a lot, but you could research the natural mutagens/phytochemicals.

You are avoiding saturated fatty acids, but you eat the worst fatty acids, PUFAs. PUFAs will oxidize with natural air, heat, and digestion. Resistant starch will ferment inside of you and cause flatulence.

Ketogenic diet is an extreme diet, I would do it if I had cancer though.

Don't wait until you're fat, sick, and nearly dead to start your health journey.

[Darryl]

Yes, PUFAs and to a lesser extent MUFAs oxidize.

 

However, the more important question is what is causing them to oxidize. And as far as I can tell, extracellular oxidation is largely a product of inflammatory superoxide generation (NADPH oxidases, zanthine oxidase etc.). We know a good deal about triggers for the inflammatory cascades upstream of those oxidases, and among the Toll-like receptor activators (for example) are long-chain saturated fats (both directly with the 16+ carbon SFAs, and through increasing intestinal permeability to endotoxins). So while there's a weak and largely theoretical advantage for SFAs in reducing the suceptiblity of LDL particles to oxidation, they fail miserably at reducing the endothelial inflammation underlying vascular disease, and systemic inflammation that contributes to most other chronic and aging-related disease. I could go on and on about the issues of long-chain SFAs and inflammation, from endotoxin import, TLR activation, inflammation, oxidative stress, endothelial function, CVD, and metabolic disorders, to dementia, etc. Its a rather consistent story, and to me indicates oxidation of LDL particles is a peripheral issue compared to the elephant in the room: systemic postprandial inflammation, caused by high long-chain SFA intake.

 

With the exception of ensuring a high eicosapenteanoic acid/arachidonic acid ratio (again, to limit inflammatory cascades), I'm not terribly fond of substantial PUFA intake either. In human and animal trials PUFA-for-SFA substitution consistently reduces CVD risk, but with the exception of coldwater fish oils and flaxseed all refined PUFAs have poor (< 1:1) ω-3/ω-6 ratios. I use spray canola and mustard oil (not terrible, at around 1:2) very sparingly.

 

Resistant starch is possibly the healthiest of all caloric sources, as it appears to have substantial benefits in intestestinal dysbiosis and is largely converted to short-chain fatty acids in the colon, a good candidate for the least problematic calories of all. In diets low in sulfur from methionine or the long-chain SFAs that require sulfur containing bile acids for emulsification, hydrogen sulfide production and flatuent odor is negligible. My personal experience is that diets with consistently high levels of resistant starch and other fermentable oligosaccharides also pose less of a volumetric concern than many have experienced with only occassional bean meals. I suspect the gut microbiota adapts to better utilize methane and hydrogen, the odorless gasses responsible for most volume. 

Edited by Darryl, 14 January 2016 - 05:28 AM.

[platypus]

Keep the Flying Spaghetti Monster out of a discussion of nutrition, please. 

[1jol1uvcaaq]

Yes, PUFAs and to a lesser extent MUFAs oxidize.

 

However, the more important question is what is causing them to oxidize. And as far as I can tell, extracellular oxidation is largely a product of inflammatory superoxide generation (NADPH oxidases, zanthine oxidase etc.). We know a good deal about triggers for the inflammatory cascades upstream of those oxidases, and among the Toll-like receptor activators (for example) are long-chain saturated fats (both directly with the 16+ carbon SFAs, and through increasing intestinal permeability to endotoxins). So while there's a weak and largely theoretical advantage for SFAs in reducing the suceptiblity of LDL particles to oxidation, they fail miserably at reducing the endothelial inflammation underlying vascular disease, and systemic inflammation that contributes to most other chronic and aging-related disease. I could go on and on about the issues of long-chain SFAs and inflammation, from endotoxin import, TLR activation, inflammation, oxidative stress, endothelial function, CVD, and metabolic disorders, to dementia, etc. Its a rather consistent story, and to me indicates oxidation of LDL particles is a peripheral issue compared to the elephant in the room: systemic postprandial inflammation, caused by high long-chain SFA intake.

 

With the exception of ensuring a high eicosapenteanoic acid/arachidonic acid ratio (again, to limit inflammatory cascades), I'm not terribly fond of substantial PUFA intake either. In human and animal trials PUFA-for-SFA substitution consistently reduces CVD risk, but with the exception of coldwater fish oils and flaxseed all refined PUFAs have poor (< 1:1) ω-3/ω-6 ratios. I use spray canola and mustard oil (not terrible, at around 1:2) very sparingly.

 

Resistant starch is possibly the healthiest of all caloric sources, as it appears to have substantial benefits in intestestinal dysbiosis and is largely converted to short-chain fatty acids in the colon, a good candidate for the least problematic calories of all. In diets low in sulfur from methionine or the long-chain SFAs that require sulfur containing bile acids for emulsification, hydrogen sulfide production and flatuent odor is negligible. My personal experience is that diets with consistently high levels of resistant starch and other fermentable oligosaccharides also pose less of a volumetric concern than many have experienced with only occassional bean meals. I suspect the gut microbiota adapts to better utilize methane and hydrogen, the odorless gasses responsible for most volume. 

 

You have no idea what you are talking about. Protein is ESSENTIAL for health, strength, energy, and stamina. Carbs are proven to be like a drug. There was a study where it was found to be MORE ADDICTIVE THAN COCAINE.

[1jol1uvcaaq]

 

Yes, PUFAs and to a lesser extent MUFAs oxidize.

 

However, the more important question is what is causing them to oxidize. And as far as I can tell, extracellular oxidation is largely a product of inflammatory superoxide generation (NADPH oxidases, zanthine oxidase etc.). We know a good deal about triggers for the inflammatory cascades upstream of those oxidases, and among the Toll-like receptor activators (for example) are long-chain saturated fats (both directly with the 16+ carbon SFAs, and through increasing intestinal permeability to endotoxins). So while there's a weak and largely theoretical advantage for SFAs in reducing the suceptiblity of LDL particles to oxidation, they fail miserably at reducing the endothelial inflammation underlying vascular disease, and systemic inflammation that contributes to most other chronic and aging-related disease. I could go on and on about the issues of long-chain SFAs and inflammation, from endotoxin import, TLR activation, inflammation, oxidative stress, endothelial function, CVD, and metabolic disorders, to dementia, etc. Its a rather consistent story, and to me indicates oxidation of LDL particles is a peripheral issue compared to the elephant in the room: systemic postprandial inflammation, caused by high long-chain SFA intake.

 

With the exception of ensuring a high eicosapenteanoic acid/arachidonic acid ratio (again, to limit inflammatory cascades), I'm not terribly fond of substantial PUFA intake either. In human and animal trials PUFA-for-SFA substitution consistently reduces CVD risk, but with the exception of coldwater fish oils and flaxseed all refined PUFAs have poor (< 1:1) ω-3/ω-6 ratios. I use spray canola and mustard oil (not terrible, at around 1:2) very sparingly.

 

Resistant starch is possibly the healthiest of all caloric sources, as it appears to have substantial benefits in intestestinal dysbiosis and is largely converted to short-chain fatty acids in the colon, a good candidate for the least problematic calories of all. In diets low in sulfur from methionine or the long-chain SFAs that require sulfur containing bile acids for emulsification, hydrogen sulfide production and flatuent odor is negligible. My personal experience is that diets with consistently high levels of resistant starch and other fermentable oligosaccharides also pose less of a volumetric concern than many have experienced with only occassional bean meals. I suspect the gut microbiota adapts to better utilize methane and hydrogen, the odorless gasses responsible for most volume. 

 

You have no idea what you are talking about. Protein is ESSENTIAL for health, strength, energy, and stamina. Carbs are proven to be like a drug. There was a study where it was found to be MORE ADDICTIVE THAN COCAINE.

When on a ketogenic diet, high cholesterol is one of the benefits. You need to do more research. It increases the healthy LDL cholesterol, not the bad one.

 

If you're so healthy, why don't you post your cronometer? Are you scared we will see your deficiences? Meat is the most nutrient dense food on the planet!

Edited by 1jol1uvcaaq, 15 January 2016 - 01:45 AM.

[Darryl]

1jol1uvcaaq, I fear you may have stumbled upon the wrong forum for your desires. This is a community where a slogan like, "Meat is the most nutrient dense food on the planet!" carries little weight. Only a few forum members are vegan, but among both the vegans and omnis here we're more apt to ask, "what nutrients" and "is there an optimal level of those nutrients for anti-aging purposes".

 

Long term members here generally know both the advantages of ketogenic diets, and the disadvantages. There's an extensive literature on problems with both ketogenic diets and less strict low-carb diets. I'm sure knowledgeable keto proponents are also aware of the issues. As several of us have mentioned above, there are certainly disease states where the potential advantages of ketogenic diets begin to outweigh known disadvantages.

 

Where longecity members go further is that we're highly focused on results from experimental gerontology, where caloric restriction, protein restriction, and methionine restriction have all repeatedly demonstrated marked anti-aging effects. Some of us are making serious efforts to apply these insights from experimental gerontology in our own n=1 experiments. We recognize that there are competing objectives involved, where for example rapid weight-loss, bodybuilding, or simply preventing sarcopenia may require different diets than delaying cellular senescence or telomere maintenance. There are compromises to be made, and probably markedly different ideal diets at different life stages.

 

 

 

 

Edited by Darryl, 15 January 2016 - 02:41 AM.

[1jol1uvcaaq]

You avoided my question. good job. you dont know a thing about longevity if you havent studied the inuit and massai

Edit: Here are some sites you can actually learn something, instead of repeating lies you heard on the internet:

http://www.marksdailyapple.com/

https://www.reddit.com/r/keto/

http://www.lowcarbfr...7f93435c40&f=91

This combines real life experiences and science.

MOST importantly you should research mucoid plaque, which is caused by starch.

I am definitely on the correct forum. I eat only 1100 calories a day to live 100+. Overeating carbs is as bad as overeating protein. I also take raw astragalus root daily and glycine to name a few of my superfoods.

People who eat high carb also have CAD. I recommend taking enzymes for that and your mucoid plaque

Edited by 1jol1uvcaaq, 15 January 2016 - 04:20 AM.

[aza]

First off again, the inuit generally were not ketogenic. Only the young masai warriors ate an all meat diet, but not for their entire lives. They may or may not have been in ketosis, it really depends on how much protein they ate and glycogen they consumed. They also drank tea, which could have helped nutrient wise. Looking at modern hunter gatherers and other members of the homo genus i can see an argument for a higher fat diet. But i certainly cant see keto as a traditional human diet, although i think it is useful for certain conditions.

 

 

[platypus]

Our ancestors would have been stupid to totally avoid carbs 100% of the time. Also, if they had done just that, sugar would not taste good to us! The great addictive taste of sugar is proof that our ancestors were exposed to carbs as an energy-source.

[Skyguy2005]

No long-lived human population has consumed a ketogenic diet. The Inuit are neither long-lived, nor particularly immune to cardiometabolic disease.

 

While it possible that humans may have better adaptations to high fat or protein diets than our fellow extant Euarchontoglires, who for the past 95 million years have almost universally eaten very low fat and moderate protein diets, in practice human populations that consume higher fat diets develop cardiometabolic disease, and those that consume higher protein diets appear to have greater cancer mortality, pretty much the pattern observed in animal experiments.

 

Solon-Biet SM et al. 2014. The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. Cell metabolism, 19(3), pp.418-430.

 

 

 

Its also true no long-lived human population has consumed a vegan diet, though some have consumed less than 5% of calories from animal sources.

 

Willcox DC et al. 2009. The Okinawan diet: health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load. Journal of the American College of Nutrition, 28(sup4), pp.500S-516S.

 

Ignoring the serious and relatively recently solved issue of B12 sufficiency, there appears little health effect of a vegan diet versus the very low animal product diets consumed in the long-lived Blue Zones (marginal issues with antigen incorporation, eg Neu5gc and related autoimmune disorders). 

 

There probably isn't going to be conclusive evidence for an ideal longevity-promoting diet in the decades those of us alive today have left to take advantage of it. We can only follow the research, and adopt diets that resemble those that reduce age-associated diseases in large human populations, especially where they are supported by evidence from long-term animal feeding trials. For me, that means a predominantly whole plant based diet, high in fiber, resistant starch, hormetic and inflammation modulating phytochemicals, and low in calorie density, long-chain saturated fats, methionine (ie animal protein), and refined carbohydrates/glycemic index/added sugars. Whether one further restricts this whole plant based diet to a (B12 supplemented!) vegan diet is more of an ethical decision than one based on health evidence.

 

I also see some role for ketogenic diets, though I see little net health benefit except in the cases of diagnosed metastatic cancer, intractable epilepsy, or morbid obesity.

 

Good post man! 

 

There seems to be a lot of evidence that out of the proteins, methionine (and maybe cysteine?) is a particularly good thing for restricting. Do we know much about why this is? 

[Darryl]

Do we know much about why this is? 

 

Methionine restriction upregulates uncoupling protein UCP1, increasing uncoupled respiration and reducing ROS production at mitochondrial complex I, increases endogenous H₂S production, and induces FGF21 signalling and the retrograde response. See this post for methionine restriction mechanism studies, and this post for methionine supplementation studies.

[1jol1uvcaaq]

 

Do we know much about why this is? 

 

Methionine restriction upregulates uncoupling protein UCP1, increasing uncoupled respiration and reducing ROS production at mitochondrial complex I, increases endogenous H₂S production, and induces FGF21 signalling and the retrograde response. See this post for methionine restriction mechanism studies, and this post for methionine supplementation studies.

 

 

The vegan diet is NOT safe. There was a 40 year old vegan who died of a heart attack.  There are other cases where vegans  face strokes, heart attacks, etc...

 

Protein deficiency is a serious problem. Amino acids are the healthiest macronutrient. Some amino acids are actually known to increase important natural antioxidants like glutathione. Free radicals are the cause of aging. By decreasing our exposure to them through ketogenic diets, we can live a healthier and longer life.

Edited by 1jol1uvcaaq, 18 January 2016 - 11:08 PM.

[Darryl]

some things

 

I don't know where you get your ideas, but its not a reliable source.

 

We know a few things about macronutrient balance and oxidative stress, namely that protein intake is posiively associated wth it.

 

Youngman LD et al. 1992. Protein oxidation associated with aging is reduced by dietary restriction of protein or calories. Proceedings of the National Academy of Sciences, 89(19), pp.9112-9116.

Sanz A et al. 2004. Protein restriction without strong caloric restriction decreases mitochondrial oxygen radical production and oxidative DNA damage in rat liver. Journal of bioenergetics and biomembranes, 36(6), pp.545-552.

Sanz A et al. 2006. Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage. Journal of bioenergetics and biomembranes, 38(5-6), pp.327-333.

Ayala et al. 2007. Dietary protein restriction decreases oxidative protein damage, peroxidizability index, and mitochondrial complex I content in rat liver. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 62(4), pp.352-360.

López-Torres M. 2008. Lowered methionine ingestion as responsible for the decrease in rodent mitochondrial oxidative stress in protein and dietary restriction: possible implications for humans.Biochimica et Biophysica Acta (BBA)-General Subjects, 1780(11), pp.1337-1347.

 

Ketogenic diets actually appear to increase free-radical production, but that's not necessarily a bad thing in light of hormesis.

 

Jain SK et al., 1998. Ketosis (acetoacetate) can generate oxygen radicals and cause increased lipid peroxidation and growth inhibition in human endothelial cells. Free Radical Biology and Medicine, 25(9), pp.1083-1088.

Jain SK et al. 1999. Effect of hyperketonemia on plasma lipid peroxidation levels in diabetic patients. Diabetes care, 22(7), pp.1171-1175.

Jain, SK et al. 2007. High glucose and ketosis (acetoacetate) increases, and chromium niacinate decreases, IL-6, IL-8, and MCP-1 secretion and oxidative stress in U937 monocytes.Antioxidants & redox signaling, 9(10), pp.1581-1590

Stadler K et al 2008. Direct evidence of iNOS-mediated in vivo free radical production and protein oxidation in acetone-induced ketosis. American Journal of Physiology-Endocrinology and Metabolism, 295(2), pp.E456-E462.

Milder JB et al. 2010. Acute oxidative stress and systemic Nrf2 activation by the ketogenic diet. Neurobiology of disease,40(1), pp.238-244.

Allen BG et al. 2013. Ketogenic diets enhance oxidative stress and radio-chemo-therapy responses in lung cancer xenografts. Clinical cancer research, 19(14), pp.3905-3913.

Kanikarla-Marie P.& Jain SK., 2015. Role of hyperketonemia in inducing oxidative stress and cellular damage in cultured hepatocytes and Type 1 diabetic rat liver. Cellular Physiology and Biochemistry,37(6), pp.2160-2170.

 

Many are personally invested in the received wisdom that protein is the "best" macronutrient. There are indeed some things that high-protein diets do well: appetite suppression and anabolic stimulation. However, insofar as increasing longevity goes, the experimental evidence suggest a protein or methionine restricted diet, though enough to avoid kwashikor or sarcopenia, is optimal.

 

Should you puruse the primariy literature, you'll find a lot of nutrients are suspect in inducing aging mechanisms. Caloric "safe-haven" macronutrients are rare, perhaps limited.to lower glycemic index and digestion resistant (higher-amylose) starches, fermentable oligosaccharides, short-chain and true (C6:0-C10:0) medium chain fatty acids, omega-3 PUFAs, and most amino acids (methionine, histidine, tyrosine, glutamate, and cysteine in excess have adverse effects, while leucine and perhaps the other BCAAs induce mTOR1, a central regulatory hub impicated in aging by rapamycin and gene knockdown studies).

Edited by Darryl, 19 January 2016 - 07:23 AM.

[1jol1uvcaaq]

 

some things

 

I don't know where you get your ideas, but its not a reliable source.

 

We know a few things about macronutrient balance and oxidative stress, namely that protein intake is posiively associated wth it.

 

Youngman LD et al. 1992. Protein oxidation associated with aging is reduced by dietary restriction of protein or calories. Proceedings of the National Academy of Sciences, 89(19), pp.9112-9116.

Sanz A et al. 2004. Protein restriction without strong caloric restriction decreases mitochondrial oxygen radical production and oxidative DNA damage in rat liver. Journal of bioenergetics and biomembranes, 36(6), pp.545-552.

Sanz A et al. 2006. Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage. Journal of bioenergetics and biomembranes, 38(5-6), pp.327-333.

Ayala et al. 2007. Dietary protein restriction decreases oxidative protein damage, peroxidizability index, and mitochondrial complex I content in rat liver. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 62(4), pp.352-360.

López-Torres M. 2008. Lowered methionine ingestion as responsible for the decrease in rodent mitochondrial oxidative stress in protein and dietary restriction: possible implications for humans.Biochimica et Biophysica Acta (BBA)-General Subjects, 1780(11), pp.1337-1347.

 

Ketogenic diets actually appear to increase free-radical production, but that's not necessarily a bad thing in light of hormesis.

 

Jain SK et al., 1998. Ketosis (acetoacetate) can generate oxygen radicals and cause increased lipid peroxidation and growth inhibition in human endothelial cells. Free Radical Biology and Medicine, 25(9), pp.1083-1088.

Jain SK et al. 1999. Effect of hyperketonemia on plasma lipid peroxidation levels in diabetic patients. Diabetes care, 22(7), pp.1171-1175.

Jain, SK et al. 2007. High glucose and ketosis (acetoacetate) increases, and chromium niacinate decreases, IL-6, IL-8, and MCP-1 secretion and oxidative stress in U937 monocytes.Antioxidants & redox signaling, 9(10), pp.1581-1590

Stadler K et al 2008. Direct evidence of iNOS-mediated in vivo free radical production and protein oxidation in acetone-induced ketosis. American Journal of Physiology-Endocrinology and Metabolism, 295(2), pp.E456-E462.

Milder JB et al. 2010. Acute oxidative stress and systemic Nrf2 activation by the ketogenic diet. Neurobiology of disease,40(1), pp.238-244.

Allen BG et al. 2013. Ketogenic diets enhance oxidative stress and radio-chemo-therapy responses in lung cancer xenografts. Clinical cancer research, 19(14), pp.3905-3913.

Kanikarla-Marie P.& Jain SK., 2015. Role of hyperketonemia in inducing oxidative stress and cellular damage in cultured hepatocytes and Type 1 diabetic rat liver. Cellular Physiology and Biochemistry,37(6), pp.2160-2170.

 

Many are personally invested in the received wisdom that protein is the "best" macronutrient. There are indeed some things that high-protein diets do well: appetite suppression and anabolic stimulation. However, insofar as increasing longevity goes, the experimental evidence suggest a protein or methionine restricted diet, though enough to avoid kwashikor or sarcopenia, is optimal.

 

Should you puruse the primariy literature, you'll find a lot of nutrients are suspect in inducing aging mechanisms. Caloric "safe-haven" macronutrients are rare, perhaps limited.to lower glycemic index and digestion resistant (higher-amylose) starches, fermentable oligosaccharides, short-chain and true (C6:0-C10:0) medium chain fatty acids, omega-3 PUFAs, and most amino acids (methionine, histidine, tyrosine, glutamate, and cysteine in excess have adverse effects, while leucine and perhaps the other BCAAs induce mTOR1, a central regulatory hub impicated in aging by rapamycin and gene knockdown studies).

 

Protein is of top importance for longevity.

http://www.scienceda...40314095102.htm

Nuts, which are high in fats and proteins, are proven to increase the longevity of humans.

There is a difference between grass-fed protein and conventional protein. Your studies are biased. Vegans are dangerous and will do anything to convert people, even if it means spreading lies through studies. This is the same thing PepsiCo and Coca-Cola are doing.

http://www.theguardi...-health-studies

Carbohydrates cause advanced glycation end products to beformed in food!

http://www.neurobiol...0143-2/abstract

 

 

Edited by 1jol1uvcaaq, 19 January 2016 - 10:47 PM.

[Darryl]

I don't doubt your first link. As I noted above, the evidence points to reducing protein or methionine significantly, but not so far as to induce sarcopenia (the term of art for geriatric muscle wasting). One of my favorite studies of the two years also went into this issue, 

 

Levine ME et al. 2014. Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population. Cell metabolism, 19(3), pp.407-417.

 

Low protein diets (<10% of E) markedly improve survival up to age 65-70, especially compared to high intake (>20% of E), but thereafter, at least moderate protein (> 10%) seems optimal. Muscle wasting probably doesn't play a causal role here. I suspect that as people grow more sedentary with age, and lower calorie intake, that <10% protein diets start to impinge upon immune system response. It should be noted that its near impossible to design a whole foods diet with <10% E as protein. The common starchy staples are > 10% E as protein, while vegetables (usually a marginal calorie source) have more protein / calorie than most animal products

 

However, I've got some decades to go before I reach that 65-70 threshold. At my age, benefits of protein (or more realistically, methionine) restriction seem to outweigh the harms. which are mostly limited to more difficulty achieving satiety or bulking muscle. There are low-calorie density/volumetrics dietary alternatives to hypothatlamic mTOR activation by leucine, and so long as I can heft steel scuba doubles, my lean mass is perfectly adequate to my desires.

 

As for nuts, for the most part they appear to benefit survival less through any fundamental aging mechanisms, than through (1) reducing sudden cardiac death via magnesium intake 2) reducing cholesterol levels via phytosterol content interfering with cholesterol reuptake, 3) providing fiber and polyphenols that beneficially modulate gut microbiota. That said, many nuts have very high Gly/Met ratios, and a popular thread here has looked into glycine supplementation, and high Gly/Met or (Gly+Ser)/(Met+Cys) ratio diets, as a means of achieving effective methionine restriction, otherwise impossible on a whole food, non junk food diet.

 

AGEs are formed in food through the Maillard reaction, which requires 1) protein, lysine residues specifically, 2) carbohydrates, especially fructose,which forms reactive carbonyl species at ten times the rate of glucose, and 3) high broiling/frying heat. It happens on the surface of roasted meats because they, too include enough sugars.

 

The most cited food AGE content reference is

 

Uribarri J. et al, 2010. Advanced glycation end products in foods and a practical guide to their reduction in the diet. Journal of the American Dietetic Association, 110(6), pp.911-916.

 

Carboxymethyllysine content is not a perfect measure of total AGE content and there are issues with the methodology (AGE, in vegetable oils?), but it offers some comparisons in broad strokes. You'll find that starchy foods aren't major culprits, unless deep fried. The worst offenders are fried and roasted meats.I'll take my Potato, white, boiled 25 min (17 AGE kU/serving) over ketogenic bacon, fried 5 min no added oil (11,905 AGE kU/serving) any day of the week.

 

Given the low AGE content of my diet, I'm more concerned with endogenous AGE formation. Pretty much all the complications of diebetes are due to too many monosaccharide-derived reactive carbonyls floating about. You can give any lab animal diebetic complications (cataracts, neuropathy, skin collagen cross-linking, kidney disorders) by feeding it enough fructose, so my fructose intake is limited to whole dark berries. I also try to keep my insulin sensitivity high and my fasting glucose low with a low long-chain saturated fat intake. Glucose 72 mg/dL in my EOY blood workup, so potatoes, bean torillas, and salads seem to be working.

 

> even if it means spreading lies through studies

Stop it. You're going to make me laugh demonically and start lovingly stroking my mustache.

 

 

 

[1jol1uvcaaq]

I don't doubt your first link. As I noted above, the evidence points to reducing protein or methionine significantly, but not so far as to induce sarcopenia (the term of art for geriatric muscle wasting). One of my favorite studies of the two years also went into this issue, 

 

Levine ME et al. 2014. Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population. Cell metabolism, 19(3), pp.407-417.

 

Low protein diets (<10% of E) markedly improve survival up to age 65-70, especially compared to high intake (>20% of E), but thereafter, at least moderate protein (> 10%) seems optimal. Muscle wasting probably doesn't play a causal role here. I suspect that as people grow more sedentary with age, and lower calorie intake, that <10% protein diets start to impinge upon immune system response. It should be noted that its near impossible to design a whole foods diet with <10% E as protein. The common starchy staples are > 10% E as protein, while vegetables (usually a marginal calorie source) have more protein / calorie than most animal products

 

However, I've got some decades to go before I reach that 65-70 threshold. At my age, benefits of protein (or more realistically, methionine) restriction seem to outweigh the harms. which are mostly limited to more difficulty achieving satiety or bulking muscle. There are low-calorie density/volumetrics dietary alternatives to hypothatlamic mTOR activation by leucine, and so long as I can heft steel scuba doubles, my lean mass is perfectly adequate to my desires.

 

As for nuts, for the most part they appear to benefit survival less through any fundamental aging mechanisms, than through (1) reducing sudden cardiac death via magnesium intake 2) reducing cholesterol levels via phytosterol content interfering with cholesterol reuptake, 3) providing fiber and polyphenols that beneficially modulate gut microbiota. That said, many nuts have very high Gly/Met ratios, and a popular thread here has looked into glycine supplementation, and high Gly/Met or (Gly+Ser)/(Met+Cys) ratio diets, as a means of achieving effective methionine restriction, otherwise impossible on a whole food, non junk food diet.

 

AGEs are formed in food through the Maillard reaction, which requires 1) protein, lysine residues specifically, 2) carbohydrates, especially fructose,which forms reactive carbonyl species at ten times the rate of glucose, and 3) high broiling/frying heat. It happens on the surface of roasted meats because they, too include enough sugars.

 

The most cited food AGE content reference is

 

Uribarri J. et al, 2010. Advanced glycation end products in foods and a practical guide to their reduction in the diet. Journal of the American Dietetic Association, 110(6), pp.911-916.

 

Carboxymethyllysine content is not a perfect measure of total AGE content and there are issues with the methodology (AGE, in vegetable oils?), but it offers some comparisons in broad strokes. You'll find that starchy foods aren't major culprits, unless deep fried. The worst offenders are fried and roasted meats.I'll take my Potato, white, boiled 25 min (17 AGE kU/serving) over ketogenic bacon, fried 5 min no added oil (11,905 AGE kU/serving) any day of the week.

 

Given the low AGE content of my diet, I'm more concerned with endogenous AGE formation. Pretty much all the complications of diebetes are due to too many monosaccharide-derived reactive carbonyls floating about. You can give any lab animal diebetic complications (cataracts, neuropathy, skin collagen cross-linking, kidney disorders) by feeding it enough fructose, so my fructose intake is limited to whole dark berries. I also try to keep my insulin sensitivity high and my fasting glucose low with a low long-chain saturated fat intake. Glucose 72 mg/dL in my EOY blood workup, so potatoes, bean torillas, and salads seem to be working.

 

> even if it means spreading lies through studies

Stop it. You're going to make me laugh demonically and start lovingly stroking my mustache.

 

Thank you for proving me right. I take daily glycine for protein. This way I keep a good gly/meth ratio and stay healthier than vegans because of the essential amino acids.

There is no point in veganism if a simple glycine supplement can fix the ratio.

Edited by 1jol1uvcaaq, 20 January 2016 - 02:18 AM.

[niner]

This being a thread about diet, we should probably remember the all-important dictum:  Don't Feed The Trolls.

[Adam Karlovsky]

 

I take daily glycine for protein. This way I keep a good gly/meth ratio and stay healthier than vegans because of the essential amino acids.

There is no point in veganism if a simple glycine supplement can fix the ratio.

He must be super healthy from consuming 60-120g of glycine a day to offset his high methionine intake. I bet glycine also does everything vegetables do, too. /sarcasm

[1jol1uvcaaq]

 

 

I take daily glycine for protein. This way I keep a good gly/meth ratio and stay healthier than vegans because of the essential amino acids.

There is no point in veganism if a simple glycine supplement can fix the ratio.

He must be super healthy from consuming 60-120g of glycine a day to offset his high methionine intake. I bet glycine also does everything vegetables do, too. /sarcasm

 

If you want to form constructive criticism to help the community, that is great. By misinforming the public that 120g of glycine is required to offset the methionine from a ketogenic diet, you are only contributing to the problem with veganism I am trying to warn others about. I'm not sure if that part was sarcastic too, but someone would need to consume thousands of calories of protein to ever eat 60g of methionine. Sarcasm and assumptions that I believe glycine replaces vegetables is not needed and serves no other purpose than to cause distress and confusion.

 

I love everybody, whether they eat ketogenic, vegan, fast food, and anywhere in between and outside of those dimensions. By labeling others trolls, we are only pushing people away from health and pushing health away from ourselves. I agree there is heat between the vegan and ketogenic communities, but my goal was to shine a light on the subject to understand longevity. If we want to improve our understanding of health, we must extinguish the biases that keep us from an open mind.

Edited by 1jol1uvcaaq, 21 January 2016 - 02:20 AM.

[sthira]

I'm a longterm vegan surrounded by many other longterm vegans. And I feel no "heat" between "the vegan and ketogenic communities..." Lol... But I will say many here in the vegan community place more emphasis on animal rights and alleviation of sentient being suffering than narrow personal human health goals. Veganism practiced well can be very very healthy; practiced poorly it can be super unhealthy.

Regarding nutrition, everyone has an opinion. What no one has is certainty as to what's best. Lack of consensus on what's healthiest remains one big ole problem. What are your goals? Is your dietary aim to make you thin? You want big muscles? To keep your bones strong? Prevent a heart attack or cancer or Alzheimer's?

With consciously practiced veganism, we're able to accomplish ALL of these personal goals AND eat a sustainable diet that's less hurtful and cruel to fellow sentient animals.

My challenge to meat eaters everywhere is to look at a cow in his big brown eyes, then humanely kill him, skin him, chop him to pieces, deal with his blood, guts, take his life, and then eat him with pleasure and humility. When your stomach is happy and full, the. responsibly dispose of his carcass. But if you as a meat eater only ever buy your cows packaged, processed, prepared from the grocery store -- and you never experience actually killing the animal with your own hands -- then I say phooey on you.

[Adam Karlovsky]

Apologies for my sarcasm. It seems you're assuming that you can offset 1g methionine with 1-2g of glycine. This is not the case when we look at rats, and I am not aware of any data on humans.

Go to this other thread where I look at the study that everyone's referring to with regard to glycine supplementation offsetting methionine intake: http://www.longecity...ine-restriction

Edited by Adam Karlovsky, 21 January 2016 - 03:46 AM.

[1jol1uvcaaq]

I'm a longterm vegan surrounded by many other longterm vegans. And I feel no "heat" between "the vegan and ketogenic communities..." Lol... But I will say many here in the vegan community place more emphasis on animal rights and alleviation of sentient being suffering than narrow personal human health goals. Veganism practiced well can be very very healthy; practiced poorly it can be super unhealthy.

Regarding nutrition, everyone has an opinion. What no one has is certainty as to what's best. Lack of consensus on what's healthiest remains one big ole problem. What are your goals? Is your dietary aim to make you thin? You want big muscles? To keep your bones strong? Prevent a heart attack or cancer or Alzheimer's?

With consciously practiced veganism, we're able to accomplish ALL of these personal goals AND eat a sustainable diet that's less hurtful and cruel to fellow sentient animals.

My challenge to meat eaters everywhere is to look at a cow in his big brown eyes, then humanely kill him, skin him, chop him to pieces, deal with his blood, guts, take his life, and then eat him with pleasure and humility. When your stomach is happy and full, the. responsibly dispose of his carcass. But if you as a meat eater only ever buy your cows packaged, processed, prepared from the grocery store -- and you never experience actually killing the animal with your own hands -- then I say phooey on you.

With a standard introduction, your story touched my heart when you shifted the topic to the suffering of animals. This has definitely been something on my mind whenever I buy my beef. I'll admit I haven't seen a lot of studies supporting meat. In fact I've seen the contrary. I'm going to be thinking about this.

 

It seems you're assuming that you can offset 1g methionine with 1-2g of glycine. This is not the case when we look at rats, and I am not aware of any data on humans.

Go to this other thread where I look at the study that everyone's referring to with regard to glycine supplementation offsetting methionine intake: http://www.longecity...ine-restriction

Thank you. I am impressed.

[sthira]

That's very cool, 1jol1uvcaaq, and rare. That is, we rarely see adults open to a change of mind. One visit to a commercial slaughterhouse usually cures people. Cures for at least a little while, anyway. Kind of like when you drive by a terrible car accident -- seeing that slows you down, makes you reconsider behavior. It's really difficult for consumers to access commercial meat processing facilities, and that's by design. "They" don't want you to see what's happening inside. That's because owners know if you do see what's happening inside you'll lose your appetite. And maybe forever.

So mental flexibility on your part -- the ability to open your mind without having experienced exposure to the casual horrors within -- is healthy.

Having said all that, though, I don't believe a vegan diet is the best human diet. It may be healthy for some people at some stages of their lives. Or maybe not. Veganism and vegetarianism do offer two big benefits, though: the non-killing of cool, interesting animals, and healthy ways to eat if practiced consciously.

[Antonio2014]

Inuits have special adaptations to their diet. For example: http://scienceblogs....ht-and-stature/